At the same time, the infection shifts the balance of receptor activator of nuclear factor κB ligand (RANKL)-mediated signaling and macrophage colony-stimulating factor, increasing osteoclast differentiation and activity [63–65], while inducing apoptosis in osteoblasts through tumor necrosis factor (TNF)-α and TRAIL (TNF-related apoptosis-inducing ligand). The gene discussed is TNFSF10; the disease is infection.